Vitamin D supplementation during pregnancy: Effect on the neonatal immune system in a randomized controlled trial.

Background: Programming of the immune system during fetal development can influence asthma-related risk factors and outcomes in later life. Vitamin D is a well-recognized immune modulator, and deficiency of this nutrient during pregnancy is hypothesized to influence disease development in offspring.

Objective: We sought to investigate the effect on neonatal immunity of maternal supplementation with 4400 IU/d vitamin D during the second and third trimesters of pregnancy by using a subset of cord blood samples from a randomized, double-blind, placebo-controlled clinical trial (the Vitamin D Antenatal Asthma Reduction Trial).

Inhibiting lung lining fluid glutathione metabolism with GGsTop as a novel treatment for asthma.

Asthma is characterized by airway inflammation. Inflammation is associated with oxidant stress. Airway epithelial cells are shielded from this stress by a thin layer of lung lining fluid (LLF) which contains an abundance of the antioxidant glutathione.

CCR4+T cell recruitment to the skin in mycosis fungoides: potential contributions by thymic stromal lymphopoietin and interleukin-16.

Mycosis fungoides (MF) is characterized by skin accumulation of CCR4+CCR7- effector memory T cells; however the mechanism for their recruitment is not clearly identified. Thymic Stromal Lymphopoietin (TSLP) is a keratinocyte-derived cytokine that triggers Th2 immunity and is associated with T cell recruitment to the skin in atopic dermatitis. Interleukin-16 (IL-16) is a chemoattractant and growth factor for CD4+T cells.

Regulation of cellular processes by interleukin-16 in homeostasis and cancer.

Interleukin-16 (IL-16) is generated as a precursor molecule that is cleaved by caspase-3 to produce a pro-IL-16 molecule that functions as a regulator of T cell growth, and a secreted peptide that functions as a CD4 and/or CD9 ligand for induction of cell motility and activation. IL-16 has been predominantly studied as a contributing factor in the orchestration of an immune response; however, more recently IL-16 bioactivity has been closely associated with the progression of a number of different cancers. While the association between IL-16 plasma levels and tumor progression has been reported for many types of cancer, the mechanism for IL-16 involvement has been partially elucidated for three of the cancer types, cutaneous T cell lymphoma (CTCL), multiple myeloma (MM), and breast cancer.

Comparison of the etiology of viral respiratory illnesses in inner-city and suburban infants.

Background: The risk of developing childhood asthma has been linked to the severity and etiology of viral respiratory illnesses in early childhood. Since inner-city infants have unique environmental exposures, we hypothesized that patterns of respiratory viral infections would also be distinct.

Methods: We compared the viral etiology of respiratory illnesses in 2 groups: a cohort of 515 infants from 4 inner-city areas and a cohort of 285 infants from mainly suburban Madison, Wisconsin.

Longitudinal relationship of early life immunomodulatory T cell phenotype and function to development of allergic sensitization in an urban cohort.

Background: Immunomodulatory T cells are thought to influence development of allergy and asthma, but early life longitudinal data on their phenotype and function are lacking.

Objectives: As part of the Urban Environment and Childhood Asthma (URECA) study, we investigated the development of immunomodulatory T cell phenotype and function, and characterized their relation to allergic disease progression from birth through to 2 years of age.

Methods: Immunomodulatory T cell phenotype and function in cord blood mononuclear cells (CBMC) and peripheral blood mononuclear cells (PBMC) at 1 and 2 years of age were characterized by analysing CD25(bright) and FoxP3(+) expression, proliferative responses and cytokine production.

Loss of nuclear pro-IL-16 facilitates cell cycle progression in human cutaneous T cell lymphoma.

Cutaneous T cell lymphomas (CTCLs) represent a heterogeneous group of non-Hodgkin lymphomas that affect the skin. The pathogenesis of these conditions is poorly understood. For example, the signaling mechanisms contributing to the dysregulated growth of the neoplastic T cells are not well defined.

A genome-wide association study of plasma total IgE concentrations in the Framingham Heart Study.

Background: Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation.

Objective: We sought to ascertain the genetic risk factors that lead to IgE dysregulation.

Methods: A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS).

Interleukin-16 as a marker of Sézary syndrome onset and stage.

Introduction: Sézary syndrome is one of the most common forms of cutaneous T cell lymphoma (CTCL). It is characterized by skin infiltration of malignant T cells. We examined interleukin-16, a potent T cell chemoattractant and cell-cycle regulator, as a prospective marker of disease onset and stage.

A homologous form of human interleukin 16 is implicated in microglia recruitment following nervous system injury in leech Hirudo medicinalis.

In contrast to mammals, the medicinal leech Hirudo medicinalis can completely repair its central nervous system (CNS) after injury. This invertebrate model offers unique opportunities to study the molecular and cellular basis of the CNS repair processes. When the leech CNS is injured, microglial cells migrate and accumulate at the site of lesion, a phenomenon known to be essential for the usual sprouting of injured axons.

Pro-IL-16 recruits histone deacetylase 3 to the Skp2 core promoter through interaction with transcription factor GABP.

Pro-IL-16 is a PDZ domain-containing protein expressed in T cells. Our previous work showed that upon activation of normal T cells, pro-IL-16 mRNA and protein are diminished in close correlation to the down-regulation of p27KIP1 protein. In addition, we showed that pro-IL-16 regulates the transcription of Skp2, the mechanism of which, however, remains elusive.

RNAIII-inhibiting-peptide-loaded polymethylmethacrylate prevents in vivo Staphylococcus aureus biofilm formation.

Staphylococci, common orthopedic pathogens, form antibiotic-resistant biofilms. Polymethylmethacrylate (PMMA) beads loaded with the quorum-sensing inhibitor RNAIII-inhibiting peptide (RIP) were implanted in rats and shown to prevent methicillin-resistant Staphylococcus aureus infection. RIP release was bimodal, typical of previously-tested antibiotics.

Cross-reactivity of human lupus anti-DNA antibodies with alpha-actinin and nephritogenic potential.

Objective: Cross-reactivity with kidney antigens is believed to be a critical determinant in the renal pathogenicity of anti-double-stranded DNA (anti-dsDNA) antibodies. Murine nephritogenic anti-dsDNA antibodies have been shown to cross-react with alpha-actinin, and anti-alpha-actinin antibodies have been found to be deposited in the kidneys of lupus mice with active nephritis. Furthermore, in humans with systemic lupus erythematosus (SLE), it has been found that a greater proportion of polyclonal IgG anti-dsDNA antibodies from patients with renal involvement bind to alpha-actinin than do those from patients without renal disease.

Strong T cell type-1 immune responses to HIV-1 Tat (1-72) protein-coated nanoparticles.

A significant emphasis has been placed on the development of adjuvants and/or delivery systems to improve both antibody production and cell-mediated immune responses. We previously reported on a novel anionic nanoparticle, which led to enhanced humoral and T helper type-1 (Th1) biased immune responses in mice when coated with cationized model antigen. Tat (1-72) is a conserved regulatory HIV-1 protein.

The Correction of Combined Immuno- and Hemopoiesis Disorders Induced by Graft-Versus-Host Reaction.

We have shown the possibility to modulate various anemic syndromes during acquired immunodeficiency differed in pathogenesis and induced by graft versus host reaction (GVHR). There are different variants of combined erythro- and immunopoiesis disorders in the semiallogeneic system DBA/2 --> B6D2F1: immunodeficiency plus hemolytic anemia and immunodeficiency plus hemolytic anemia plus immunocomplex glomerulonephritis. In the allogeneic system C57BL/6 --> BALB/c there is immunodeficiency plus hypoplastic anemia with reduced bone marrow erythropoiesis.

Production of Peptide of Retroviral Origin in Sera of Patients with Chronic Myeloid Leukemia at Acute Phase.

In the present study we investigated production of the peptide of retroviral origin in patients with various types of leukemia. For this purpose the high affinity rabbit antibodies were generated against the synthetic peptide representing the "immunosuppressive motif" within the envelope protein of human endogenous retrovirus type C. The presence of this peptide was identified only in sera of the patients with chronic myelo- and/or promonocytic leukemia at acute phase.

Autoantibodies to amyloid beta-peptide (Abeta) are increased in Alzheimer's disease patients and Abeta antibodies can enhance Abeta neurotoxicity: implications for disease pathogenesis and vaccine development.

Studies of amyloid precursor protein transgenic mice suggest that immune responses to amyloid beta peptide (Abeta) may be instrumental in the removal of plaques from the brain, but the initial clinical trial of an Abeta vaccine in patients with Alzheimer s disease (AD) was halted as the result of serious neurological complications in some patients. We now provide evidence that AD patients exhibit an enhanced immune response to Abeta and that, contrary to expectations, Abeta antibodies enhance the neurotoxic activity of the peptide. Serum titers to Abeta were significantly elevated in AD patients and Abeta antibodies were found in association with amyloid plaques in their brains, but there was no evidence of cell-mediated immune responses to Abeta in the patients.

[In vitro synthesis of immunoglobulins caused by an inactivated Ebola virus].

An in vitro model Ebola infection was used to study the humoral response of human mononuclear cells to stimulation by purified inactivated Ebola virus antigen. Inactivated Ebola virus was cocultivated with human mononuclear cells in the presence or absence of B-cell mitogen LPS E. coli: B5.

[Effect of Ebola virus antigen on proliferative response of human lymphocytes in vitro: imbalance in production of tumor necrosis factor alpha and interleukin-1].

An in vitro model infection caused by Ebola virus (EV) showed a high production of tumor necrosis factor-alpha by human peripheral lymphocytes concurrently with a simultaneous reduction in the synthesis of interleukin-1 in response EV antigen stimulation. This may be an important factor in that VE suppresses the body's immunological resistance, which in turn causes unterferon deficiency and suppresses the formation of T helper cells.

Suppressive effect of Ebola virus on T cell proliferation in vitro is provided by a 125-kDa GP viral protein.

Ebola virus (EV), an extremely infectious pathogen, causes severe hemorrhagic fever in humans and nonhuman primates. The disease pattern includes damage of parenchymal cells of vital organs in association with hemostatic and immune disorders. Vaccination with the inactivated virions does not provide an effective immune protection against the disease.